Cochlear nuclei neuroplasticity after auditory nerve and cochlea removal

Abstract

Hearing loss clearly alters the function and connectivity in auditory pathways in the brain. The effects of an auditory receptor lesion on the auditory pathway might be linked to the absence of peripheral stimulation on the first level of the auditory pathway (cochlear nuclei, CN). Loss of stimulation affects the pathway connectivity, at least in the CN, inducing the reorganization of the neural circuits. This reorganization may reduce the efficiency of some deafness therapies, including cochlear implants. Cochlea removal has been shown to be a good model for analysing neuroplasticity in the CN. Three main periods of degeneration and regeneration were found after cochlea removal. During the first week after cochlea removal, early effects included auditory nerve fibre degeneration, and the progressive degeneration of nerve endings on CN neurons. Some CN neurons degenerate. From the second week after cochlea removal a very limited and diffuse expression of GAP-43, a protein linked to developing or regenerating axon growth cones, was found. Expression was observed in small nerve endings connecting cochlear nuclei neurons. One month after cochlea removal, CN were stabilized with a clear reduction of new neuron degeneration. At this time a very relevant expression of GAP-43 was found around remaining neurons, in particular in the ventral cochlear nuclei. Molecular aspects and control of neuroplasticity in cochlear nuclei still remains controversial, even though it is clear that trophic factors and many other substances (i.e. neurotransmitters) have been involved in neuroplasticity.